Cocaine abuse
Cocaine is a stimulant and a local anesthetic with potent vasoconstrictor properties. Leaves of the coca plant (Erythroxylon coca) contain 1 to 1.5 percent cocaine. The drug is marketed illicitly in the form of a white crystalline powder, usually adulterated with lactose or glucose to 50 percent purity. Frequently cocaine is adulterated with other local anesthetics such as lidocaine, procaine, and tetracaine. Cocaine’s biologic effects result from alteration and blockade of cellular membrane transport, particularly prevention of the reuptake of biogenic amines, an effect shared with the tricyclic antidepressants.
Prevalence of cocaine use Cocaine is expensive in comparison to most other illicit drugs and has attained the reputation of a “status” drug in western industrialized societies. The actual extent of illicit cocaine use is unknown, but there is evidence of a recent escalation in the United States. The Drug Abuse Warning Network (DAWN) reported that emergency room mentions of cocaine abuse increased by 75 percent from 1981 through the fourth quarter of 1983. During the first quarter of 1984, approximately 2000 cocaine mentions were reported, a number equal to all the cocaine mentions for the full year of 1978. A National Household Survey conducted in 1982 revealed that 21.6 million persons had tried cocaine at least once, a dramatic increase from the 5.4 million who reported at least one use of cocaine during 1974. The most prevalent pattern of use in America appears to be occasional, sporadic intake of relatively low doses of cocaine.
Acute and chronic cocaine intoxication The most common mode of cocaine self-administration is by inhalation or “snorting,” where the drug is rapidly absorbed from the nasal mucosa and produces a brief, dose-related stimulation and enhancement of mood. Cardiac rate and blood pressure also increase in a dose-related manner. An increase in body temperature usually occurs following cocaine administration, and high doses of cocaine may induce lethal pyrexia or hypertension. Because cocaine inhibits reuptake of catecholamines at adrenergic nerve endings, the drug potentiates sympathetic nervous system activity. During recent years smoking of coca paste (a product produced by extracting cocaine preparations with flammable solvents) has become increasingly popular. Administration of the drug via intravenous injection also occurs more frequently. Cocaine has a short plasma half-life of approximately 1 h. In humans, cocaine is primarily metabolized by plasma esterases, and cocaine metabolites are excreted in urine. The very short duration of euphorigenic effects of cocaine observed in chronic abusers is probably due to both acute and chronic tolerance. Frequent self-administration of the drug (2 to 3 times per hour) is often reported by chronic cocaine abusers. Modulation of both the cocaine “high” and the abrupt dysphoric disappearance of cocaine’s effects with alcohol is often reported.
The prevalent assumption that cocaine use is relatively safe is challenged by reports of death from respiratory depression, cardiac arrhythmias, and convulsions after cocaine snorting and intravenous administration. Severe pulmonary disease may develop in individuals who smoke coca paste; this is attributed both to the direct effects of cocaine and to residual solvent contaminants in the smoked material. Numerous clinical reports, dating from the late nineteenth century, strongly suggest that protracted cocaine abuse may induce paranoid ideation and visual and auditory hallucinations, a state which resembles alcoholic hallucinosis. Psychological dependence upon cocaine, as manifested by inability to abstain from frequent compulsive use, has also been reported. Although occurrence of withdrawal syndromes involving psychomotor agitation and autonomic hyperactivity remains controversial, severe depression (”crashing”) may be a concomitant of drug withdrawal.
Treatment of cocaine intoxication and abuse Treatment of cocaine overdose is a medical emergency which involves resuscitation in an intensive care unit. Cocaine toxicity produces hypertension, tachycardia, tonic-clonic seizures, dyspnea, and ventricular arrhythmias. Intravenous diazepam in doses up to 0.5 mg/kg administered over an 8-h period has been shown to be effective for control of seizures. The systemic concomitants of a hypermetabolic state produced by cocaine toxicity with concurrent ventricular arrhythmias have been managed successfully by administration of 0.5 to 1.0 mg of propranolol intravenously. Since many instances of cocaine-related mortality have also been associated with concomitant use of other illicit drags (particularly heroin), the physician must be prepared to institute effective emergency treatment for multiple drug toxicity.
Treatment of chronic cocaine abuse requires combined efforts by family physicians, psychiatrists, and psychosocial care providers. Early abstinence from cocaine use is often complicated by symptoms of depression and guilt, insomnia, and anorexia, which may be as severe as those observed in major affective disorders. Individual and group psychotherapy, family therapy, and peer group assistance programs are often useful for inducing prolonged remission from drug use. Preliminary reports suggest that both lithium treatment and tricyclic antidepressant medication may be of value for the long-term treatment of cocaine abuse, even when affective disorder or depression are not present. In fact, depressive illness does not appear to be a frequent antecedent of cocaine abuse.